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3D week 3 - hormones 2 > pituitary disease (see DM) > Flashcards

pituitary disease (see DM) Flashcards

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
Q

gigantism vs acromegaly

A

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)

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26
Q

clinical effects of GH deficency on children

A

short stature

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27
Q

clinical effects of GH deficency on adults (3)

A
  1. abnormal body composition
  2. reduced muscle mass
  3. reduced well being and performance
28
Q

clinical effects of LH deficency in men (2)

A
  1. hypogondism
  2. reduced sperm count
29
Q

clinical effects of LH deficency in women (3)

A
  1. hypogonadism
  2. amenorrhoea
  3. oligomenorrhoea
30
Q

clinical effects of FSH deficency

A

infertility

31
Q

clinical effects of TSH deficency

A

hypothyroidism

32
Q

clinical effects of ACTH deficency

A
  1. loss of pigmentation
  2. hypoadrenalism
33
Q

clinical effects of prolactin deficency

A

failure of lactation (rare except in sheehan’s syndrome)

34
Q

clinical effects of ADH deficency

A

diabetes insipidus

35
Q

what is the characteristic order that horones fail in

A

GH -> LH -> FSH -> TSH -> ACTH -> PRL

36
Q

how to treat hyper-prolactinism

A

give DA agonists (they inhibit prolactin release)

37
Q

why do prolactin levels rise if there is disruption to the pituitary stalk

A

hypothalamus can’t check the levels and so there is nothing regulating the prolactin levels => they rise

38
Q

5 causes of overactive pituitary gland

A

development of a functioning tumour:
1. cushing’s disease
2. acromegaly
3. prolactinoma
4. TSHome (rare)
5. gonadotrophinoma (usually acts like non functioning)

39
Q

what is a functioning tumour

A

a tumour that causes abnormally large amounts of hormones to be released into the bloodstream

40
Q

when in the day should cortisol levels be checked

A

9am or in a stress response

41
Q

when in the day should testosterone levels be checked

A

in the morning after fasting

42
Q

what should the result of a dexamethasone test be

A

undetectable levels of cortisol due to -ve feedback

43
Q

which hormone level often rises as all other hormone levels fall in disease

A

prolactin

44
Q

what is seen in the plasma GH levels in obese patients

A

loss of peaks and troughs -> loss of pulsatilty

45
Q

what kind of test should be done for pulsatile hormone

A

24hr collection test

46
Q

what hormones does an insulin stress test check for

A

low levels of GH or ACTH

47
Q

what hormones does a glucagon stress test check for

A

low levels of GH or ACTH

48
Q

what does a synacthen test check for

A

low cortisol levels

49
Q

treatment for non-functioning pituitary tumours (3)

A
  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
Q

what is the preferred method of pituitary surgery

A

trans-sphenoid surgery - it leaves no scar

51
Q

how should hyrocortisone be prescribed

A

at specific times to mimic circadian dose rather than TDS -> highest dose at waking and last dose no later than 18:00

52
Q

what is desmopressin

A

a synthetic analog of vasopressin/ADH -> used to control urine output and thirst

53
Q

what will oestrogen HRT help women with

A

reduces menopause effects like flushing and weakening of bones

54
Q

what needs to be monitored if men are taking testosterone HRT (5)

A
  1. testosterone levels
  2. FBC
  3. PSA
  4. LFT
  5. rectal exam
55
Q

GH deficency comorbidities (5)

A
  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
Q

what is the best treatment for functioning tumours and what is the execption

A

surgery, except for prolactinomas where DA agonists are the most effective

57
Q

what are the 5 most common functioning tumour conditions (endo)

A
  1. prolactinoma
  2. acromegaly
  3. cushing’s
  4. TSHoma
  5. GNoma
58
Q

what is prolactinoma and what does it lead to

A

tumour of the lactotroph cells -> results in high prolactin which leads to amenorrhoea and galactorrhoea

59
Q

why do women often present earlier with prolactinomas than men

A

more noticable symptoms -> periods stop

60
Q

who are prolactinoma common in

A

young women

61
Q

what kind of prolactinomas are more common in men

A

macroprolactinomas (>1cm) -> present with hypogonadism typically

62
Q

cushing’s disease vs syndrome

A

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
Q

treatment for TSHoma (2)

A
  1. surgery
  2. somatostain analogues
64
Q

what is pituitary apoplexy

A

sudden haemorrhage of the pituitary gland -> usually into an existing pituitary tumour

65
Q

pituitary apoplexy presentation (5)

A
  1. sudden headache
  2. vomiting
  3. collapse
  4. visual field loss
  5. ophthalmoplegia (eye muscle paralysis)
66
Q

pituitary apoplexy mgx

A
  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
Q
A

3D week 3 - hormones 2 (6 decks)

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