pituitary Flashcards

1
Q

diabetes insipidus

A

a lack of diuretic hormone (ADH) or lack of response to ADH

–> prevent kidneys from being able to concentrate urine leading to polyuria + polydipsia

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2
Q

types of diabetes insipidus

A

nephrogenic - collecting ducts of kidneys do not respond to ADH

cranial - hypothalamus does not produce ADH for the pituitary gland to secret

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3
Q

causes of nephrogenic diabete insipidus

A

drugs - lithium (used in bipolar affective disorder)
intrinsic kidney disease
electrolyte disturbance - hypOkalaemia + hypercalcaemia

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4
Q

mutation in what gene can cause nephrogenic diabetes?

A

AVPR2 gene on X chromosome that codes for ADH receptor

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5
Q

presentation of diabetes insipidus

A

polyuria + polydipsia
dehydration
postural hypotension
hypernatremia

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6
Q

what is the water deprivation test (desmopressin stimulation test) ? what is it used to diagnose?

A

diabetes insipidus / primary polydipsia

patient avoids fluid for 8hrs, urine osmolality measured 
synthetic ADH (desmopressin) is given
8hrs later urine osmolality measured again

(different results for each nephrogenic, cranial + primary polydipsia)

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7
Q

diabetes insipidus management

A

treat underlying cause, if mild manage conservatively

demopressin (synthetic ADH) - for both, higher dose in nephrogenic (monitor closely)

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8
Q

dibetes insipidus investigations

A

low urine osmolality
high serum osmolality
water deprivation test = test of choice

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9
Q

water deprivation test urine osmolality results in cranial diabetes insipidus

A

after deprivation = low

after ADH = high

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10
Q

water deprivation test urine osmolality results in nephrogenic diabetes insipidus

A

after deprivation = low

after ADH = low

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11
Q

water deprivation test urine osmolality results in primary polydipsia

A

after deprivation + after ADH given both = high

primary polydipsia = when the patient has a normally functioning ADH system but they are drinking excessive quantities of water leading to excessive urine production. They don’t have diabetes insipidus.

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12
Q

what is hypopituitarism physiologically due to?

A

inability of pituitary gland to provide sufficient hormones due to -

  • inability of pituitary to produce hormones
  • insufficent supply of hypothalamic-releasing hormones
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13
Q

causes of hypopituitarism

A

pituitary tumours
local brain tumours - meningioma, glioma, craniopharyngiomas
infiltrative processes - sarcoidosis
infections - cerebral abscesses, meningitis
trauma - head injury
autoimmune
iatrogenic/surgery

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14
Q

hypopituitarism presentation

A

huge spectrum - depends on severity, hormones predominantly involved

mentrual irregularities
gynaecomastia in males
abdominal obesity
loss of facial, axillary or pubic hair
dry skin + hair
growth retardation
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15
Q

risk of testosterone replacement

A

polycythaemia = high conc of RBCs in blood
–> risk of stroke/MI, monitor

prostate enlargement - not cancer
hepatitis

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16
Q

what is cushing’s syndrome?

A

prolonged elevation of cortisol

causes protein loss

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17
Q

whats the difference between cushing syndrome + cushing disease?

A

syndrome = prolonged elevation of cortisol

disease = where pituitary adenoma secretes excessive ACTH

disease causes syndrome but sundrome not always caused by disease

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18
Q

causes of cushing syndrome

A

long term steroid use
pituitary adenoma secreting excessive ACTH (cushings disease)
adrenal adenoma (hormone secreting adrenal tumour)
paraneoplastic - ectopic ACTH (small cell lung cancer)

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19
Q

presentation of cushings syndrome

A
round moon face
central obesity
thin, weak limbs
abdominal striae
buffalo hump - fat pad on back
frontal balding in women
conjunctival oedema (chemosis)

osteoporosis
easy brusing + poor skin healing

high stress hormone levels

  • hypertension
  • cardiac hypertrophy
  • hyperglycaemia - T2DM
  • depression
  • insomnia
20
Q

cushings syndrome investigations

A

dexamethsone suppression test - overnight or over couple days, positive if cortisol not suppressed

24hr free cortisol
MRI of brain - pituitary adenoma
chest CT - small cell lung cancer
abdo CT - adrenal tumours

21
Q

management of cushing syndrome

A

remove underlying cause - ectopic, transphenoidal for pituitary tumour

if fails reove but adrenal glands + give replacement steroid hormone for life

metryapone

22
Q

pharmacological management of cushings syndrome

A

metryrapone - if others fail or while waiting for radiotherapy to work

23
Q

what does a pituitary adenoma releasing excessive ACTH cause?

A

Cushings disease –> cushing syndrome - prolonged elevation of cortisol

24
Q

presentation of prolactinoma

A

female

  • EARLY presentation
  • galactorrhoea (milky nipple discharge)
  • menstrual irregularity
  • amenorrhoea (lack of periods)
  • infertility

male

  • LATE presentation
  • impotence
  • abnormal visual field
  • anterior pituitary malfunction
25
Q

prolactinoma investigations

A

wraised serum prolactin
MRI of pituitary
check visual field
pituitary function tests - other hormones affected

26
Q

pathological causes of raised prolactin

A

hypothyroidism
stalk lesions - iatrogenic, road accident
prolactinoma (prolactin secreting tumour)

27
Q

drugs that increase prolactin

A

drugs that inhibit dopamine (antagonists) - antiemetics (metoclopramide)

antipsychotics
antidepressants

28
Q

physiological causes of a raised prolactin

A

breast feeding
pregnancy
stress
lack of sleep

29
Q

management of prolactinomas

A

dopamine agonists = cabergoline (dostinex)
- 1/2 times a week oral

others = bromociptine, quinagolide

v successful - tumour shrinkage, pregnancy/menstruation, normal prolactin

30
Q

side effects of dopamine agonists

A

N+V
low mood
fibrosis (in high doses)

31
Q

cause of acromegaly

A

excessive growth hormone
commonest cause = pituitary adenoma

can be secondary to lung/pancreatic cancer that secretes ectopic growth hormone releasing hormone (GHrH) or GH (rare)

32
Q

acromegaly presentation

A
prominent forehead + brow
large nose, tongue, jaw
headaches - vascular
skin tags
profuse sweating
bitemporal hemianopia
arthritis - imbalanced growth of joints
hypertrophic heart
hypertension
T2DM
33
Q

what conditions does acromegaly increase the risk of?

A

colorectal cancer - colonic polyps

early CV death

34
Q

acromegaly investigations

A

insulin-like growth factor (IGF-1) - raised
OGTT while measuring GH (high glucose usually suppresses growth hormone)

MRI brain - pit tumour
ophthalmology - visual field testing
check other pit hormones

*random GH level not useful - fluctuates

35
Q

management of acromegaly

A

surgery = definitive, remove source

pharmalogical

  • somatostatin analogues - ocreotide
  • dopamine agonists - bromocriptine
  • pegvisomant
  • somatostatin + dopamine has inhibitory effect on GH release
  • somatostatin = more potent
36
Q

somatostatin analogues

A

ex = ocreotide
blocks GH release - acromegaly treatment

– shrinks tumour in most, used pre-op

SE = abdo pain, diarrhoea, gall stones

37
Q

what inhibits growth hormone release?

A

somatostatin + dopamine

38
Q

causes of SIADH

A

post-operative
infection - atypical pneumonia, lung abscesses
head injury
medications - thiazide diuretics, carbamazepine, antipsychotics, NSAIDs
malignancy - small cell lung cancer
meningitis

39
Q

medication that can cause SIADH

A
thiazide diuretics
carbamazepine
antipsychotics
NSAIDs
sulfonylureas
SSRIs
40
Q

Anti-diuretic hormone (ADH) function

A

produced in the hypothalamus + secrete in the posterior gland of the pituitary

ADH stimulates water reabsorption from collecting ducts in the kidneys

also know as vasopressin

41
Q

pathophysio of SIADH

A

excessive ADH results in excessive water reabsorption in the collecting ducts
–> this water dilutes the sodium in the blood = hyponatraemia

(reabsorption not big enough to cause fluid overload = euvolemia hyponatraemia)

urine becomes more concentrated - urine osmalality + urine sodium high

42
Q

syndrome of inappropriate diuretic hormone presentation

A

severe hypOnatraemia

  • seizures
  • reduced consciousness

non-specific

  • headache, fatigue
  • muscle aches + cramps
  • confusion
43
Q

SIADH investigations

A

hyponatraemia
high urine sodium
high urine osmolality
euvolemia

exclude other causes of hyponatraemia
establish cause - chest x-ray

44
Q

SIADH managment

A

correct sodium - SLOW, prevent central pontine myelinolysis
fluid restriction might be enough to correct

tolvaptan (‘vaptans’) = ADH receptor blockers

demeclocycline (tetracycline antibiotic) = inhibits ADH

45
Q

complication of SIADH

A

central pontine myelinolysis (osmotic demylination)
–> long term hyponatraemia being treated too quickly

osmosis causes brain to swell