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Endocrine > Pituitary > Flashcards

Pituitary Flashcards

1
Q

What hormones are secreted by the anterior pituitary?

A

GH, PRL, TSH, FSH, LH, ACTH, Beta-lipotrophin

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2
Q

What is the action of GH?

A
  1. stimulates the liver to produce insulin-like growth factor 1
  2. increases lipolysis
  3. increases hepatic glucose production
  4. decreases tissue glucose uptake
  5. increases protein synthesis
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3
Q

How is GH release stimulated?

A

IGF-1 exerts negative feedback at the pituitary where it modulates the release of GHRH.
Negative feedback of IGF-1 and GH at the hypothalamus modulate somatostatin release

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4
Q

How do you test for GH excess (acromegally)

A

Oral glucose tolerance test - GH secretion is inhibited by hyperglycaemia so GH levels should be low if there is normal pituitary function. If there is acromegally, GH will not be suppressed.

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5
Q

How do you test for GH deficiency?

A

GH stimulation test: Insulin hypoglycaemia test

  • peak plasma conc <20mU/L is reliable for diagnosis of GH deficiency.
  • IGF-1 plasma level is often performed first and if low, then an IHT performed (safer).
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6
Q

When do GH levels peak?

A

sporadic bursts mainly during sleep

stimulated by stress, exercise, hypoglycaemia

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7
Q

How is prolactin secretion controlled?

A

Pulastile secretion - increases during stress and sleep

Negative action of dopamine secreted by the hypothalamus

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8
Q

What defines a macroprolactinoma and why is this important?

A

PRL > 6000 or >1cm

Despite visual symptoms can still be treated with medical therapy 1st line

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9
Q

What is the treatment for a prolactinoma?

A

Can monitor microprolactinomas if no symptoms - 95% will not enlarge
1st line treatment is dopamine agonists
- cabergoline or bromocriptine

Only if no response - consider surgery

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10
Q

What are the symptoms of a prolactinoma?

A

Galactorrhoea, Oligomenorrhoea, Infertility, Lack of Libido, Erectile Dysfunction, Long term risk low BMD

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11
Q

What happens to prolactin in pregnancy?

A

PRL secretion in women is dependent on oestrogen status
Rises during pregnancy
Levels fall to normal within 7 days after delivery if not breast feeding, and begin to decline after 3 months if breastfeeding

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12
Q

Why would you do an insulin tolerance test?

A

To assess GH and ACTH reserve
The stress associated with hypoglycaemia should cause an increase in cortisol and an increase in GH.
In a normal ITT: cotrisol > 580, GH > 20

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13
Q

What are the treatments for acromegaly?

A
  1. transphenoidal surgery
  2. radiotherapy - if failed surgery or unsuitable candidate
  3. Medical therapy
    - somatostain analogues (octreotide_
    - Dopamine agonist (cabergoline/bromocriptine)
    - GH receptor agonists (Pegvisomant)
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14
Q

What is the incidence of Cushing’s disease?

A

2/million
3-15:1 F:M
commonest at 20-40 years

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15
Q

What is the mortality of untreated Cushing’s disease?

A

30-50% at 5 years

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16
Q

What is the most common cause of Cushing’s disease?

A

Pituitary ACTH corticotroph microadenoma

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17
Q

What clinical feature is most associated with Cushing’s disease?

A

Proximal muscle weakness

18
Q

Why would you perform a short synacthen test?

A

To assess adrenocortical function and ACTH reserve

- in a normal test (normal adrencortical axis) the cortisol should rise to >580

19
Q

How is ACTH secreted?

A

Diurnal variation

  • peaks at ~0800
  • lowest at ~midnight
  • negative feedback by cortisol
  • increased by stress
20
Q

What disease states cause elevated ACTH secretion?

A
  • ACTH secreting pituitary tumour (Cushing’s disease)
  • Primary adrenal failure (Addison’s disease)
  • Ectopic secretion by non-pituiatary tumours
21
Q

Name some drugs that can cause hyperprolactinaemia

A

Antipsychotics, methyldopa, oestrogens

22
Q

What are the initial tests to investigate for Cushing’s syndrome?

A
  1. Establish that there is in fact raised cortisol
    - 24 hour urinary cortisol N < 50
    - Overnight Dex supp test*
    (Dexamethasone is not detected on cortisol assay, whereas Prednisone is)
    - midnight salivary cortisol (midnight cortisol levels should low)
23
Q

What can interfere with serum cortisol levels?

A

Exogenous oestrogens

24
Q

How do you diagnose Cushing’s disease once elevated cortisol levels have been established?

A
  1. ACTH levels
    - very high in ectopic secretion
    - moderately elevated in CD
    - low in adrenal tumour (neg feedback)
  2. High dose Dex supp test
    - 2mg Dex given 6 hourly over 48 hours
    - 0900 cortisol taken after last dose
    - CD - cortisol drops to <50%
    - Ectopic/adrenal tumour - no suppression
  3. CRH test
    - CRH given: in CD ACTH increases by 50%and cortisol by 20% after 1 hour
    - no response in ectopic ACTH secretion or adrenal tumour
  4. MRI pituitary
  5. Inferior Petrosal Sinus sampling if MRI normal
25
Q

What is the treatment for Cushing’s disease?

A
  1. Transphenoidal resection
  2. Pituitary radiotherapy
  3. Bilateral adrenalectomy -last resort
  4. Metyrapone is used as a bridging therapy whilst awaiting surgery (blocks cortisol synthesis by reversibly inhibiting steroid 11β-hydroxylase)
26
Q

What hormones are released by the posterior pituitary?

A

Vasopression (ADH)

Oxytocin

27
Q

What are the causes of cranial diabetes insipidus?

A
  1. Familial
    - autosomal dominant, DIDMOAD (DI, DM, optic atrophy and deafness)
  2. Acquired
    - trauma
    - tumours
    - inflamm: sarcoid, TB, Langerhan cell histicytosis
    - infection: meningitis, encephalitis
    - vascular: sheehans syndrome, sickle cell
28
Q

What are the causes of nephrogenic DI?

A
  1. Familial
    - X-linked recessive, autosomal recessive
  2. Acquired
    - drugs: Lithium
    - Met: hyper Ca & glycaemia, hypo K
    - CRF
    - Post-obstructive uropathy
29
Q

How do you investigate for DI?

A
  1. 24 hour urine - confirm >3L/day output
  2. Random urinary osmolality > 750 excludes diagnosis
  3. Exclude DM and RF, met cause
  4. Water deprivation test + response to vasopressin
  5. MRI
30
Q

How do you differentiate between DI and primary polydipsia and cranial from nephrogenic DI?

A

Water deprivation test tells all!

  • first 8 hours of water deprivation tests ability to concentrate urine (not possible with DI - dilute urine, rise in plasma osmolality)
  • response to vasopression afterwards tests the kidney’s ability to respond to vasopressin (in NDI, kidneys are resistant to DDAVP so urine remains dilute, in CDI the urine concentrates)
31
Q

How do you treat CDI?

A

Allow access to fluid

DDAVP nasal spray

32
Q

How do you treat NDI?

A

Allow access to fluid

Thiazide diuretics

33
Q

What is the role of Vasopressin?

A

controls water excretion by altering the permeability of the renal collecting tubules to water in response to changes in extracellular fluid osmolality

34
Q

Causes of hypopituitarism

A
  1. Developmental/genetic - eg kallmans, prader willi, dysplasia
  2. Acquired
    - pituitary neoplams
    - hypothalamic neoplasm
    - trauma - surgery, radiation, head injury
    - infiltrative disease - sarcoid, haemochromatosis, amyloid
    - lymphocytic hypophysitis
    - pituitary apoplexy
    - empty sella
35
Q

What order does hormone production fail?

A 
GH (falls first)
FSH
LH
TSH
ACTH

Adults first sign will be hypogonadism
Children first sign will be growth retardation

36
Q

Hormone replacement in hypopituitarism

A

ACTH - hydrocortisone 10-20mg mane and midi, 5-10mg nocte
TSH - thyroxine
FSH/LH - males = testosterone, females = estrogen/progsterone
GH - GH supplement
Vasopressin - desmopressin

37
Q

What percentage of pituitary tumours secrete what?

A 
Non functioning - 40%
Prolactinoma - 30%
GH secreting - 15%
ACTH secreting 10%
TSH or FSH secreting - 5%
38
Q

What is difference between micro and macroadenomas?

A

Microadenomas

  • less than 1cm
  • most common, usually incidentaloma, seen in 15% of population

Macroadenomas

  • greater than 1cm
  • most common cause of hypopituitarism
  • majority are non secreting
39
Q

What is a craniopharyngioma

A

Benign, suprasella cystic mass
Causes hypopituitarism (in 90%) by growing down into stalk
Surgery is mainstay of treatment but poor survival due to recurrence

40
Q

Symptoms of sellar mass

A

Bitemporal hemianopia
Headache
Diplopia
Pituitary apoplexy
Symptoms of raised prolactin - due to loss of negative dopamine feedback
Symptoms of hormone deficiency or hormone production

41
Q

Surgical indications for pituitary tumour

A
  • functional hormone secreting adenoma except prolactinoma - 1st line is medical tx
  • macroadenoma >1cm
  • hypopituitarism
  • compressive/local symptoms
42
Q

Complications of pituitary surgery

A 
Hypocortisolism
Diabetes insipidus
SIADH
Residual adenoma
Visual impairment - usually returns in 80%
Hormone deficiency

Endocrine (6 decks)

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