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Semester 1- CEP > The Pituitary Gland > Flashcards

The Pituitary Gland Flashcards

1
Q

where is the pituitary gland?

A

Sits in a bony cavity at the base of the brain called the Sella Turcica

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2
Q

what components is the pituitary gland made of?

A

Consists of two lobes:
anterior and posterior

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3
Q

what is the name of the stalk that connects the pituitary to the hypothalamus?

A

the infundibular stalk

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4
Q

what is the difference between the anterior and posterior pituitary gland?

A

The anterior lobe produces and releases hormones.
The posterior lobe does not produce hormones —this is done by nerve cells in the hypothalamus—but it does release them into the circulation

they also have different embryological origin

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5
Q

what hormones are in the anterior pituitary gland?

A

○ TSH – thyroid hormone synthesis & secretion
○ ACTH – adrenal corticosteroid synthesis
○ FSH/LH – egg/sperm development
○ GH – longitudinal growth
○ prolactin – breast milk production

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6
Q

what hormones are in the posterior pituitary gland?

A

○ ADH – water balance/osmolality
○ oxytocin – parturition (delivery of foetus/lactation)

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7
Q

what does the hypothalamus do?

A

The hypothalamus is the final common pathway by which signals from multiple systems reach the anterior pituitary gland

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8
Q

what 3 nuclei does the hypothalamus consist of?

A

Its endocrine functions are mainly regulated by paraventricular, supraoptic and ventromedial nuclei.

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9
Q

what hormone does the supraoptic nucleus produce?

A

Antidiuretic hormone (ADH)

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10
Q

what hormone does the paraventricular nucleus produce?

A

oxytocin

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11
Q

what non-endocrine functions does the hypothalamus have?

A

regulation of body temp, thirst and food intake, and blood pressure

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12
Q

what is the hypothalamuses functions regulated by?

A
  • hormone-mediated signals- (like negative feedback)
  • neural inputs- (mediated by neurotransmitters like acetylcholine, dopamine, norepinephrine, epinephrine, serotonin, GABA)
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13
Q

where in the body does the hypothalamus send signals to?

A

It sends signals to other parts of nervous system (eg. in brain stem, vasopressinergic neurons involved in autonomic regulation of BP – similar neurons project to gray matter, implicated in higher cortical functions)

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14
Q

how many nerve cells does the hypothalamus- pituitary consist of?

A

2 sets

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15
Q

what do the 2 sets of nerve cells in the hypothalamus- pituitary do?

A

1) One set sends hormones it produces down its axon, through the infundibular stalk- enters posterior lobe and goes to its axon terminal
2) The other set produce stimulating and inhibiting hormones that flow down blood vessels in the infundibular stalk and reach the anterior lobe.

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16
Q

what regulates the GH in the hypothalamus?

A

GH releasing hormone (GHRH) -stimulates the secretion
somatostatin & dopamine- inhibits the secretion

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17
Q

what regulates the FSH and LH in the hypothalamus?

A

Gonadotropin releasing hormone (GnRH)- stimulates the secretion
Prolactin - inhibits the secretion

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18
Q

how does prolactin inhibit FSH and LH?

A

Inhibits gonadal activity through central GnRH suppression which results in decreased FSH/LH- acts as natural contraceptive

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19
Q

what are common pituitary diseases?
what are their most common outcomes?

A

Sellar or Parasellar lesions cause mass effects.
Mass effects: When brain structures are compressed and injured due to the degree of space that leaking blood, cerebrospinal fluid, or edema (swelling) takes up within the restricted skull space.
The most common outcomes of these mass effects are:
Neurological effects
Visual effects
Hypopituitarism (defective secretion of pituitary hormones)
Hormone hypersecretion caused by an adenoma (benign tumour)
NB: pituitary adenoma can be non-function as well.

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20
Q

what are the neurological and visual mass effects of pituitary diseases?

A

Visual effects are caused because the optic chiasm is located right above the pituitary gland
Neurological effects are caused as lateral to the pituitary gland we have various cranial nerves.
Pressure effects on these can cause optic nerve damage or cranial nerve damage:
CNIII, IV, V, VI compression/damage (contained within cavernous sinus)
CNII damage - compression of optic chiasm causes bitemporal heterogenous hemianopia (vision is missing in the outer half of both the right and left visual field)
If the lesion exerts pressure in any direction you will get a head ache
If the lesion exerts pressure downward to sinusoid sinus - you get CSF leak
If the lesion is large enough to exert pressure up to the hypothalamus you get hypothalamic damage or brain damage

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21
Q

what is Hypopituitarism?
major causes?

A

defective secretion of pituitary hormones
Major Causes:
Hypothalamic releasing hormone deficiency (e.g Kallmann’s syndrome)
Trauma
Pituitary/Para-pituitary tumours
Radiotherapy of the pituitary or brain due to a tumour can cause the pituitary itself to be affected by radiation
Pituitary apoplexy (bleeding or impaired blood supply of the pituitary) caused by death of an infarction or Sheehan’s syndrome
Infiltration of the pituitary by inflammatory cells (sarcoidosis) or iron(haemochromatosis)

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22
Q

what are functioning pituitary adenomas?

A

Benign tumour at pituitary gland which hyper-secretes one or more hormones
If these adenomas are large enough, they will exert pressure effects e.g. on the optic pathway causing vision problems.

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23
Q

what is GH?
stimulated/ supressed by?
what does it cause/ stimulate?

A

released throughout your life
stimulated by hypoglycaemia, exercise, sleep
Supressed by Hyperglycaemia
has a pulsatile manner of secretion (see graph) - levels are usually undetectable throughout the day
It causes secretion of insulin-like growth factors (IGFs) in the liver
Its effects are controlled/carried out by these IGF-1:
Cause cartilage growth
tissue growth
Bone growth
Action on bone growth plates causes linear growth in children
Stimulates:
protein synthesis
lipolysis
increase in blood glucose
Important for Psychological well-being

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24
Q

what are GH deficiency manifestations?

A

manifestations:
children: poor growth - dwarfism
adults:
increased abdominal fat and decreased lean body mass
decreased muscle strength & exercise capacity
impaired cardiac function
impaired lipid profile
impaired psychological well-being

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25
Q

how do you diagnose GH deficiency?

A

Because GH has a pulsatile manner of secretion so stimulation tests are required to detect deficiency.
To stimulate GH: You perform an ITT (insulin tolerance test).
Inject insulin to lower blood glucose - GH released (along with cortisol) as stress response to hypoglycaemia
Then measure GH levels during various times and if GH is not above a specific level the patient is diagnosed with GH deficiency.
NB: Glucagon, GHRH + Arginine can also be used to stimulate GH release to test for deficiency.
Also measure IGF-1 levels (not gold standard as it can be normal with people with GH deficiency)

26
Q

treatment for GH deficiency?

A

hormone replacement therapy, inject recombinant GH at night to mimic body physiology

27
Q

what are the symptoms and clinical features of excess GH?

A

Often due to pituitary tumour
Increased levels of GH results in increased IGF-1 production in the liver - increased growth of both soft & hard tissue
Leads to gigantism if onset as a child or acromegaly if onset as an adult
Symptoms:
hyperhidrosis (excessive sweating)
aching of joint (osteoarthritis)
headaches
Snoring
Sleep apnoea – breathing stops in the night due to overgrowth of tissue in throat
Clinical features:
spade-like hands
broad nose
thick lips
brow protrusion
wide chin
skin thickening

28
Q

how do you diagnose GH excess?

A

Measure IFG-1 (high in cases of acromegaly)
Also do an oral glucose tolerance test.
High blood glucose levels supress GH. So if the patient has acromegaly GH will not be supressed as it is secreted by a tumour which does not listen to feed back.
Also perform pituitary imaging for the tumour
(The average diagnostic delay is around 5 years as changes are so slow or people may attribute them to aging.)

29
Q

treatment for excess GH?

A

Surgical removal of tumour
Radiotherapy
Medication - somatostatin analogues and dopamine agonists (inhibit the secretion of growth hormone by the tumour)
GH receptor antagonists (does not allow receptor to function)

30
Q

what is the function of FSH and LH?

A

Men: effect produced in the testes - promotes production of sperm & testosterone (puberty)
women: effect produced in the ovaries - promotes production of oestrogens, maturation and release of egg follicles
The FSH/LH hormones levels fluctuate during menstrual cycle with levels being higher close to ovulation. The combination of FSH, LH, Oestrogen, and Progesterone are responsible for controlling menstrual cycle.

31
Q

manifestations of FSH/LH Deficiency?
specific manifestations in women?

A

manifestations:
children: delayed puberty
men:
decreased libido
impotence (erectile dysfunction)
infertility
osteoporosis (bone disease)
decreased muscle mass & strength
Decreased 2nd sex features
Decreased mood and well-being
Anaemia
Women:
decreased libido
menstrual disorders
infertility
osteoporosis
dyspareunia (= painful sexual intercourse due to lack of oestrogen)
premature atherosclerosis

32
Q

how to diagnose FSH/LH deficiency?

A

Women: Test for decreased FSH, LH, oestradiol levels (and menstrual history)
Men: FSH, LH, and morning testosterone levels (as it is higher in the morning so it is chose reference point)

33
Q

treatment for FSH/LH deficiency?

A

Men: Testosterone replacement
Women: Oestrogen and/or progesterone replacement until menopause

34
Q

what are manifestations of excess FSH/LH?

A

manifestations:
infertility
ovarian hyperstimulation
testicular enlargement
menstrual disorder

35
Q

how to diagnose excess FSH/LH?

A

hormonal tests
pituitary imaging

36
Q

treatment for excess FSH/LH?

A

surgery
radiotherapy

37
Q

what is prolactin?

A

Essential for breast milk production - levels vastly increase in pregnancy & during breast feeding
Inhibits gonadal activity through central GnRH suppression which results in decreased FSH/LH - acts as natural contraceptive
Mainly causes disease when in excess

38
Q

what are the physiological and pathological causes of excess prolactin?

A

Physiological:
Stress
Pregnancy and lactation
Antipsychotics
Sleep
Drugs: dopamine antagonistic, antipsychotics or prolactinomas

Pathological:
Prolactinoma
Hypothalamic tumour
Primary hypothyroidism
Cranial irradiation

39
Q

what is prolactinoma?

A

A benign tumour of pituitary gland secreting large amounts of prolactin
manifestations:
hypogonadism – reduction in hormonal output of gonads
galactorrhoea – spontaneous flow of milk from breast

40
Q

how to diagnose for prolactinoma?

A

involves exclude other causes of high prolactin and pituitary imaging

41
Q

treatment for prolactinoma?

A

Dopamine agonists can cause rapid decrease in prolactin (inhibits prolactin secretion) & dramatically shrink pituitary adenoma tissue (can cause regaining of vision due to released pressure on optic nerves)
Surgery
Radiotherapy

42
Q

what is the function of ACTH?

A

Causes the release of glucocorticoids (i.e. cortisol) from the zona fasciculata of the adrenal gland & weak androgens from zona reticularis
Cortisol:
helps us respond to stress and defend the body against infections,
regulates metabolism of glucose, lipids
You have higher levels in the morning and they gradually they drop to a point where they are undetectable when we are fast asleep.
Decreased ACTH causes the adrenal gland to become atrophic (shrivelled) and excess causes hyperplasia (enlargement)

43
Q

what are the manifestations of cortisol deficiency?

A

Leads to secondary adrenal insufficiency (adrenal hypofunction)
Manifestations of cortisol deficiency:
Anorexia
weight loss
Fatigue & muscle weakness
hypoglycaemia
hypotension (low BP)
nausea/vomiting
Anaemia

44
Q

how do you diagnose cortisol deficiency?
what are dynamic tests?

A

measure 9am serum cortisol & ACTH (cortisol is higher during the morning) however this does not confirm deficiency so you need to supplement this with a dynamic test
dynamic tests:
Short Synacthen test (not in recent onset disease) – measurement of serum cortisol before & after injection of synthetic ACTH
Insulin tolerance test – inject insulin –> causes hypoglycaemia which the body sees as stress so cortisol is released. Measure cortisol levels at different intervals. If there is deficiency cortisol concentration will not reach required levels. (Used to assess HPA axis integrity; gold-standard but risks of Myocardial infarction & seizures)
Glucagon test

45
Q

treatment for cortisol deficiency?

A

Steroid hormone replacement therapy (give glucocorticoids but not aldosterone)
Higher dose in the morning then give two loser doses e.g. at 1pm then 5 pm or one dose at 2pm - mimics natural rhythm of cortisol secretion.

46
Q

what does excess cortisol cause?

A

Cushing’s syndrome: excess cortisol production
ACTH Dependent:
Corticotroph Adenoma results in hypersecretion of ACTH which goes to adrenal glands - hypersecretion of cortisol
Ectopic secretion of ACTH/CRH by a tumour somewhere else in the body
ACTH-independent:
Iatrogenic (induce by treatment): due to administration of steroids (to help with conditions like asthma) or adrenal disease (adenoma, carcinoma, hyperplasia)

47
Q

what are the manifestations of cushings syndrome?

A

Fat – central obesity, moon face, buffalo hump (fat growth on shoulder)
Skin – thin, fragile, purple striae, slow healing of cuts, acne, excessive hairiness
Psychological: Depression, anxiety, decreased libido
Reproductive:
Females: irregular or absent menstrual periods
Males: erectile dysfunction

48
Q

how to diagnose cushings syndrome?

A

24hr urine free cortisol (UFC) which is usually at high levels if a patient has cortisol excess
Midnight serum/salivary cortisol - elevated cortisol in Cushing’s (undetectable for normal person);
Low dose dexamethasone suppression test:
Give the steroid dexamethasone which is recognised by hypothalamus and pituitary as a steroid.
In human with no cushioning it will cause negative feedback which means that the steroid will reduce secretion of CRH and ACTH and so reduce cortisol production.
In patient with Cushing’s feedback does not exist so cortisol is still at high levels.
You can then perform further differential diagnostic tests to see cause of excess cortisol e.g. is it ACTH dependent or not:
- Measure 9am ACTH to see if it is ACTH dependent
- High dose Dexamethasone Suppression test
- CRH test,
- Inferior petrosal sinus sampling
- Imaging (pituitary, adrenals, chest etc.)

49
Q

treatment for cushings syndrome?

A

Surgically remove tumour
Radiotherapy of tumour
Drugs to inhibit production of cortisol for non-surgery candidates (i.e. metyrapone, ketoconazole, mitotane)
Bilateral adrenalectomy (take out adrenal glands) patient will remain hypo-adrenal, if the tumour is left behind in pituitary it may increase in size and secrete even more ACTH

50
Q

what is TSH?

A

Stimulates the thyroid to release thyroid hormone by thyroid gland
More T4 released than T3
Diurnal (day) secretion

51
Q

what are the manifestations of TSH deficiency?

A

Manifestations:
constipation
bradycardia
weight gain
Fatigue
Muscle weakness
cold intolerance
inability to lose weight
puffiness,
pale & dry skin,

52
Q

how to diagnose TSH defiency?

A

measure serum TRH, TSH, freeT4 & freeT3 levels (all low in pituitary failure)

53
Q

treatment for TSH deficiency?

A

hormone replacement (levothyroxine)

54
Q

what are the manifestations for excess TSH?

A

manifestations:
Hyperthyroidism
thyrotoxicosis
mass effects

55
Q

how to diagnose excess TSH?

A

hormonal tests (i.e. serum TRH, TSH, fT4 & fT3 levels)
pituitary imaging

56
Q

treatment for excess TSH?

A

surgery,
radiotherapy
medications (i.e. thyrostatics – antithyroid drugs that inhibit production of thyroid hormones)

57
Q

what is the function of ADH?

A

RELEASED BY POSTERIOR PITUITARY
Also known as AVP
Polypeptide hormone
Synthesised mainly in supraoptic nuclei of hypothalamus - secretory granules migrate down axons of supraoptic hypophyseal tract into the posterior lobe
ADH is the primary physiological determinant of the rate of free water excretion
Increased ADH = increased water retention
Binding of ADH to the V2 receptor in the kidneys causes upregulation of aquaporins (proteins in luminal membrane) allowing for movement of water out of the cortical and medullary collecting tubules
Major stimuli for ADH secretion - deprival of fluids:
Hyperosmolality: increased solute potential of blood –> causes thirst and causes release of ADH
Decreased effective circulating volume (e.g. due to a haemorrhage) –> leads to low BP –> ADH lvl in the blood increase.

58
Q

what does ADH deficiency cause?

A

Deficient secretion of ADH is called central diabetes insipidus
Causes of DI:
idiopathic (autoimmune destruction of hormone secreting cells)
Familial:
Autosomal dominant, mutations in AVP (ADH) gene
Wolfram (DIDMOAD) syndrome: autosomal recessive genetic disorder. It has incomplete penetrance. It also causes DM, optic atrophy and deafness
Tumours
Neurosurgery or Trauma
Infiltrative disorders e.g. sarcoidosis (collection of inflammatory cells)
Infections (meningitis, encephalitis, etc.)
Hypoxic encephalopathy or severe ischaemia

59
Q

what are the manifestations of ADH defiency?

A

polyuria (urine output > 3l/day for (adults) or > 2l/m2 (children) of dilute urine) polydipsia,
nocturia (wake up at night to urinate)
Polyuria can also be caused by diabetes Meletus and renal failure, or polydipsia so you need to be careful.

60
Q

how to diagnose ADH deficiency?

A

Measure urine output,
Measure osmolalities (plasma, urine)
measure blood electrolytes
measure glucose levels to exclude DM
blood creatinine/urea (exclude kidney disfunction),
If above are not helpful you can perform a water deprivation test (deprival of fluid). In DI polyuria will continue.

61
Q

treatment for ADH deficiency?

A

ADH analogues to resolve polyuria and avoid the consequences of dehydration.

62
Q

what is oxytocin?
function?

A

stimulates contraction of smooth muscle of breast & uterus
It is under positive feedback control
Roles in
milk ejection reflex (neuro-endocrine)
Parturition (birth) - synthetic oxytocin given to induce labour

Semester 1- CEP (16 decks)

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