pituitary disease (see DM) Flashcards

(67 cards)

1
Q

where is the pituitary gland located anatomically

A

it sits in a saddle-shaped bony cavity of the sphenoid bone, known as the sella turcica; The optic chiasma lies directly superior to the anterior pituitary

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2
Q

what can suprasella extensions of the pituitary gland result in

A

bitemporal hemianopia (compression of the optic chiasm)

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3
Q

what strucutre can parasella extensions of the piuitary gland affect

A

cavernous sinus

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4
Q

what is the appearnace of the posterior pituitary gland on an MRI

A

bright spot posterior to the ant pituitary - it is physiologically hyperdense; there should be no bright spot in the anterior pituitary

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5
Q

what is the anatomy of the posterior pituitary gland (2)

A
  1. direct extension of the hypothalamus
  2. The posterior lobe is connected to the median eminence of the hypothalamus by the pituitary stalk (also known as the infundibulum)
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6
Q

how does the posterior pituitary gland release hormones

A
  1. Neurosecretory cells in the hypothalamus synthesise hormones that are transported along axons that terminate in the posterior pituitary
  2. hormones are then released into capillaries within the posterior pituitary gland to affect body parts directly
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7
Q

how are hormones released from the anterior pituitary

A

hormones are secreted from the hypothalamus and travel via hypophyseal portal vessels to the anterior pituitary, where they regulate the release of anterior pituitary hormones into the blood

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8
Q

what is the embryological origin of the posterior pituitary gland (3)

A
  1. the infundibulum of the diencephalon which grows inferiorly - This is composed of neuroectoderm and forms the neurohypophysis
  2. The neurohypophysis is therefore in direct communication with the hypothalamus
  3. Axons from neurosecretory cells in the hypothalamus grow inferiorly into the pituitary stalk and terminate in the posterior pituitary gland
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9
Q

what is the embryological origin of the anterior pituitary gland (3)

A
  1. An outgrowth of the primitive oral cavity known as Rathke’s pouch, which grows superiorly -This is composed of ectoderm and forms the adenohypophysis
  2. The anterior pituitary is not in direct contact with the hypothalamus
  3. As the connection to the primitive mouth is lost, nests of epithelial cells may be left behind -> Occasionally these cells are functional and secrete ectopic hormones (e.g. craniopharygioma) but are usually benign
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10
Q

what hormones are not under -ve feedback control

A
  1. prolactin
  2. oxytocin (+ve feedback)
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11
Q

why does prolactin not have a feedback loop

A

no mediator gland

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12
Q

why are FSH levels high in menopause

A

oestrogen levels are low and so FSH increases to try and compensate

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13
Q

what should be checked in a pt w a hx of fainting and salt craving

A

cortisol and ACTH levels (addison’s disease) - low cortisol high ACTH in compensation

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14
Q

what hormone should be checked if acromegaly is suspected

A

IGF-1 (related to GH)

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15
Q

what is the new name for diabetes insipidus

A

Arginine Vasopressin Deficiency/resistance

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16
Q

what inhibits prolactin

A

dopamine

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17
Q

what does somatostatin inhibit

A

growth hormone

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18
Q

how can the pituitary gland malfunction (3)

A
  1. gland enlargement/ tumour with local effects
  2. gland stops working
  3. gland becomes overactive
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19
Q

what will compression of the cavernous sinus present with

A

facial pain

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20
Q

signs of pituitary gland enlargement/tumour (4)

A
  1. headaches (increased pressure)
  2. LOC/fits (increased pressure)
  3. facial pain
  4. optic involvement(e.g. bitemporal hemianopia, optic atrophy)
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21
Q

what does a supra+paracellular extension look like on an MRI

A

“snowman” appearance around midline inferiorly (coronal view)

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22
Q

what can cause the pituitary gland to stop working (8)

A
  1. non functioning pituitary tumour
  2. apoplexy
  3. hypophysitis
  4. empty sella
  5. other parasellar cysts/tumours
  6. post surgery/ radiotherapy/ cancer treatment
  7. post brain injury or hypotension (e.g. Sheehan’s)
  8. congenital/genetic
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23
Q

what is Sheehan’s syndrome

A

postpartum hypopituitarism caused by necrosis of the pituitary gland -> usually the result of severe hypotension or shock caused by massive hemorrhage during or after delivery;
may lead to continued amenorrhoea postpartum or infertility

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24
Q

causes of hypopituitarism (11)

A
  1. isolated deficency of pituitary hormones (e.g. Kallmann’s syndrome)
  2. Pit-1 deficency
  3. infective (e.g. basal tb, syphilis)
  4. vascular (e.g. pituitary apoplexy, carotid artery aneuyrsms)
  5. immunological (piuitary antibodies)
  6. neoplastic - mostly benign (e.g. carniophayngioma, hypothalmic tumour, glioma etc.)
  7. traumatic (e.g. skull fracture at base, surgery)
  8. infiltrations (e.g. sarcoidosis, hypophysitis)
  9. radiation damage
  10. empty sella syndrome
  11. functional (starvation, anorexia, emotional deprivation)
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25
gigantism vs acromegaly
gigantism - growth hormone hypersecretion occurs before the fusion of the long bone epiphysis (i.e. in children) acromegaly - GH hypersecretion occurs after the fusion of the epiphysis leading to large extremities and characteristic facies (i.e. in adults)
26
clinical effects of GH deficency on children
short stature
27
clinical effects of GH deficency on adults (3)
1. abnormal body composition 2. reduced muscle mass 3. reduced well being and performance
28
clinical effects of LH deficency in men (2)
1. hypogondism 2. reduced sperm count
29
clinical effects of LH deficency in women (3)
1. hypogonadism 2. amenorrhoea 3. oligomenorrhoea
30
clinical effects of FSH deficency
infertility
31
clinical effects of TSH deficency
hypothyroidism
32
clinical effects of ACTH deficency
1. loss of pigmentation 2. hypoadrenalism
33
clinical effects of prolactin deficency
failure of lactation (rare except in sheehan's syndrome)
34
clinical effects of ADH deficency
diabetes insipidus
35
what is the characteristic order that horones fail in
GH -> LH -> FSH -> TSH -> ACTH -> PRL
36
how to treat hyper-prolactinism
give DA agonists (they inhibit prolactin release)
37
why do prolactin levels rise if there is disruption to the pituitary stalk
hypothalamus can't check the levels and so there is nothing regulating the prolactin levels => they rise
38
5 causes of overactive pituitary gland
development of a functioning tumour: 1. cushing's disease 2. acromegaly 3. prolactinoma 4. TSHome (rare) 5. gonadotrophinoma (usually acts like non functioning)
39
what is a functioning tumour
a tumour that causes abnormally large amounts of hormones to be released into the bloodstream
40
when in the day should cortisol levels be checked
9am or in a stress response
41
when in the day should testosterone levels be checked
in the morning after fasting
42
what should the result of a dexamethasone test be
undetectable levels of cortisol due to -ve feedback
43
which hormone level often rises as all other hormone levels fall in disease
prolactin
44
what is seen in the plasma GH levels in obese patients
loss of peaks and troughs -> loss of pulsatilty
45
what kind of test should be done for pulsatile hormone
24hr collection test
46
what hormones does an insulin stress test check for
low levels of GH or ACTH
47
what hormones does a glucagon stress test check for
low levels of GH or ACTH
48
what does a synacthen test check for
low cortisol levels
49
treatment for non-functioning pituitary tumours (3)
1. replace hormones - cortisol must be replaced that day but others can wait 2. surgery 3. radiotherapy - particularly for recurrent or residual tumours post surgery
50
what is the preferred method of pituitary surgery
trans-sphenoid surgery - it leaves no scar
51
how should hyrocortisone be prescribed
at specific times to mimic circadian dose rather than TDS -> highest dose at waking and last dose no later than 18:00
52
what is desmopressin
a synthetic analog of vasopressin/ADH -> used to control urine output and thirst
53
what will oestrogen HRT help women with
reduces menopause effects like flushing and weakening of bones
54
what needs to be monitored if men are taking testosterone HRT (5)
1. testosterone levels 2. FBC 3. PSA 4. LFT 5. rectal exam
55
GH deficency comorbidities (5)
1. change in body habitus 2. reduced exercise capacity 3. change in mental state 4. worse CVD profile -> increased risk of mortality 5. reduced QOL
56
what is the best treatment for functioning tumours and what is the execption
surgery, except for prolactinomas where DA agonists are the most effective
57
what are the 5 most common functioning tumour conditions (endo)
1. prolactinoma 2. acromegaly 3. cushing's 4. TSHoma 5. GNoma
58
what is prolactinoma and what does it lead to
tumour of the lactotroph cells -> results in high prolactin which leads to amenorrhoea and galactorrhoea
59
why do women often present earlier with prolactinomas than men
more noticable symptoms -> periods stop
60
who are prolactinoma common in
young women
61
what kind of prolactinomas are more common in men
macroprolactinomas (>1cm) -> present with hypogonadism typically
62
cushing's disease vs syndrome
disease - ACTH-producing pituitary tumor leading to high cortisol levels and cushing's symptoms syndrome - set of symptoms that results when there is a surplus of cortisol in the body
63
treatment for TSHoma (2)
1. surgery 2. somatostain analogues
64
what is pituitary apoplexy
sudden haemorrhage of the pituitary gland -> usually into an existing pituitary tumour
65
pituitary apoplexy presentation (5)
1. sudden headache 2. vomiting 3. collapse 4. visual field loss 5. ophthalmoplegia (eye muscle paralysis)
66
pituitary apoplexy mgx
1. give emergency hydrocortisone if unstable or if biochemistry abnormal 2. emergency pituitary surgery if pt ha vision loss of deteriorating LOC 3. conservative mgx if present with VF or cranial nerve involvement and symptoms improve with steroids
67