Pituitary gland disorders Flashcards

(26 cards)

1
Q

explain the characteristics of the pituitary gland

A

-two lobes, anterior and posterior
-lies below the brain in the sella turcica
-the anterior lobe 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 gland.

dual blood supply:
1) long and short pituitary arteries
2) hypophyseal portal circulation which begins as a capillary plexus around the Arc.
-pituitary cell type were originally classified by their staining characteristics with acidic and basic dyes

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2
Q

explain anterior pituitary hormones and posterior pituitary hormones

A

Anterior pituitary hormones:
-ACTH; regulates the adrenal cortex
-TSH; controls production of thyroid hormones from the thyroid
-GH; controls growth
-LH/FSH; reproductive control
-PRL; breast milk production

Posterior pituitary hormones:
-ADH; water regulation (retains water)
-Oxytocin; breast milk production

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3
Q

explain the nomenclature of pituitary and hypothalamic hormones

A

-Gonadotrophin; stimulates the gonads
-Growth hormone/somatotrophin; stimulates growth
-Thyrotrophin; stimulates thyroids
-Corticotrophin; stimulates the adrenal cortex

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4
Q

explain the different layers of the endocrine system

A

1) Primary- end organ, secondary- pituitary and tertiary- hypothalamus.
2) testing for diseases begins with end organ
3) hypothalamus intergrates information and pituitary amplifies the signals
4) hypothalamus intergrates signals from the higher centres and then releases hormones that say stress/attraction, hunger etc.
5) the hypothalamus is too small to dump all the hormones into blood so it puts hormones into the portal vessels which go the pituitary gland. The pituitary dilutes the hormones and then circulates them around the body
6) peripheral hormones switch off central hormones as soon as the response starts

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5
Q

explain clinical presentation of pituitary tumours

A

Clinical presentation of pituitary tumours:
-hormone hypersection by tumours
-space occupying lesion where tumour affects nearby regions resulting in headaches, visual loss, cavernous sinus invasion
-hormone deficiency status where the tumour squishes the normal pituitary surrounding it leading to decreased hormone release from those parts.

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6
Q

explain how tumours of the anterior pituitary can cause syndromes of hormone excess

A

GH= acromegaly (gigantism)
ACTH= Cushing’s disease
TSH= secondary thyrotoxicosis
LH/FSH= Non functioning pituitary tumour
PRL= prolactinoma (pituitary gland tumour)

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7
Q

explain the actions of growth hormone

A

-GH causes the release of IGF-1 from the liver which acts on the bones (chondrocytes grow and lie down more cartilage) causing linear growth.
-to grow you need energy, lipids need to be metabolised and protein synthesised, these metabolic effects are mediated by GH itself

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8
Q

explain systemic effects of GH/IGF-1 excess (acromegaly)

A

-acral enlargement; spade like hands, increase show size, macroglossia, carpal tunnel syndrome
-increased skin thickness
-increased sweating
-skin tags
-changed apperance
-visceral enlargement

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9
Q

explain metabolic changes of GH/IGF-1 excess (acromegaly)

A

-impaired fasting glucose
-impaired glucose intolerance
-diabetes mellitus
-insulin resistance
-increased TAG

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10
Q

Explain other consequences of excess of GH/IGF-1 (acromegaly)

A

-cardiomyopathy
-hypertension
-bowel polyps (can become maligant, because GH causing increased growth)
-colonic cancer
-multinodular goitre (enlarged thyroid gland)
-hypogonadism
-arthopathy (inflammation of joints)

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11
Q

explain actions of cortisol

A

Actions of cortisol:
-increased plasma glucose levels
-increases gluconeogenesis, glycogenesis and glycogen storage
-decrease glucose utilisation
-increases lipolysis which provides energy
-proteins are catabolised to release AA
-Na+ and H20 retention maintains BP
-anti-inflammatory
-increased gastric acid production

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12
Q

explain changes in protein and fat metabolism in Cushing’s syndrome

A

-change in body shape
-central obesity
-moon face
-buffalo hump
-thin, easily bruised skin
-brittle bones
-diabetes

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13
Q

explain changes in sex hormones in cushing’s syndrome

A

-excess hair growth
-irregular periods
-problems conceiving
-impotence

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14
Q

explain salt and water retention in cushing’s syndrome

A

-high blood pressure
-fluid retention

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15
Q

explain Prolactinomas (common)

A

-Prolactin release is different to other hormones because its stimulated by mechanical stimulation of the breast rather than internal signals
-there’s an intrinsic high production of prolactin which is then inhibited
-tonic release of dopamine which is produced in the hypothalamus and travels to the pituitary inhibits the release of prolactin
-positive feedback; mechanical stimulation signals the brain to cause an instant surge in prolactin production and milk release —> this is stopped by removing the baby

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16
Q

explain non functional pituitary tumours

A

-305 of all pituitary tumours (syndrome of hormone excess isn’t produced)
-symptoms are due to space occupation such as headache, visual field defects and nerve palsies. they may interfere with the rest of pituitary function leading to defiency of hormones.
-treatment is surgery and or radiotherapy

17
Q

explain visual field defects

A

-predators have eyes in front to allow for depth vision
-nasal retina and temporal retina look at the same thing but produce slightly different images
-these neurones cross over and intergrate information for interpretation.
-pituitary gland tumour expansion damages the point chasm and all its neurons. This means we cannot see from certain regions.
-the first point to get destroyed is the bottom of the regina so the first place we lose vision is from the upper part

18
Q

explain the loss of pituitary function with an expanding tumour

A

loss of pituitary function with an expanding tumour:
-the order that we lose pituitary hormones is based on the biological importance of them:

1) LH/FSH= sex/reproduction is least priority
2) GH= growth
3) TSH= metabolism
4) ACTH= last to go as stress response is important in survival

19
Q

explain the treatment of pituitary adenomas and causes of pituitary failure

A

Treatment of pituitary adenomas:
-surgery; transphenoidal surgery, Nelson’s syndrome
-radiotherapy; slow
-drugs; block hormone production or release (somatostatin analogues as somastastin has complimentary enzymes so a short life)

causes of pituitary failure:
-tumours (benign and malignant)
-trauma
-infection

20
Q

explain what happens when thyroid hormones are low in hypopituitarism

A

Thyroid:
-bradycardia
-weight gain
-cold intolerance
-hypothermia
-constipation

21
Q

what happens if sex steroids are low in hypopituitirism

A

-oligomenorrhoea
-reduced libido
-hot flushes
-reduced body hair

22
Q

explain what happens when there is reduced cortisol in hypopituitarism

A

-tiredness
-weakness
-anorexia
-postural hypotension
-myalgia (muscle pain)

23
Q

explain reduced GH in hypopituitirism

A

-tired
-central weight gain

24
Q

explain hypopituitism treatment

A

-thyroid; thyroxine
-sex steroids; testosterone, oestrogen
-reduced cortisol; hydrocortisone
-reduced GH; growth hormone

25
explain vasopressin control and action
control: -increased plasma osmolarity detected by osmoreceptors in the hypothalamus -decreased blood pressure detected by baroreceptors -reduced PaO2 and increased PaCO2 and cortisol, sex steroids and ang II in the blood Action: -increase the permeability of the collecting ducts for water by adding aquaporins -free water is reabsorbed -vasoconstriction
26
explain syndrome is inappropiate ADH (SIADH) and diabetes insipidus
Syndrome of inappropiate ADH (SIADH): -excess ADH is released due to brain injury/infection or lung cancer/ infection -it can have metabolic causes Diabetes insipidus: -underproduction of ADH due to cranial causes (lack of production) or nephrogenic (produced but receptors non functional due to kidney damage) -polyuria-lots of urine -polydipsia- increases Na+ and plasma osmolality and reduces urine osmolality and urine Na+ -normal people can reabsorb water to produce concentrated urine unlike those with diabetes